Predicting de-novo portal vein thrombosis after HCV eradication: A long-term competing risk analysis in the ongoing PITER cohort.
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Kondili Loreta A, Zanetto Alberto, Quaranta Maria Giovanna, Ferrigno Luigina, Panetta Valentina, Calvaruso Vincenza, Zignego Anna Linda, Brunetto Maurizia R, Raimondo Giovanni, Biliotti Elisa, Ieluzzi Donatella, Iannone Andrea, Madonia Salvatore, Chemello Liliana, Cavalletto Luisa, Coppola Carmine, Morisco Filomena, Barbaro Francesco, Licata Anna, Federico Alessandro, Cerini Federica, Persico Marcello, Pompili Maurizio, Ciancio Alessia, Piscaglia Fabio, Chessa Luchino, Giacometti Andrea, Invernizzi Pietro, Brancaccio Giuseppina, Benedetti Antonio, Baiocchi Leonardo, Gentile Ivan, Coppola Nicola, Nardone Gerardo, Craxì Antonio, Russo Francesco Paolo, PITER Collaborating Investigators
Аннотация
METHODS: Patients with HCV-related cirrhosis, consecutively enrolled in the multi-center ongoing PITER cohort, who achieved the SVR using DAAs, were prospectively evaluated. Kaplan-Meier and competing risk regression analyses were performed.
RESULTS: During a median time of 38.3 months (IQR: 25.1-48.7 months) after the end of treatment (EOT), among 1609 SVR patients, 32 (2.0%) developed de novo PVT. A platelet count ≤120,000/μL, albumin levels ≤3.5 mg/dL, bilirubin >1.1 mg/dL, a previous liver decompensation, ALBI, Baveno, FIB-4, and RESIST scores were significantly different (p < 0.001), among patients who developed PVT versus those who did not. Considering death and liver transplantation as competing risk events, esophageal varices (subHR: 10.40; CI 95% 4.33-24.99) and pre-treatment ALBI grade ≥2 (subHR: 4.32; CI 95% 1.36-13.74) were independent predictors of PVT. After HCV eradication, a significant variation in PLT count, albumin, and bilirubin (p < 0.001) versus pre-treatment values was observed in patients who did not develop PVT, whereas no significant differences were observed in those who developed PVT (p > 0.05). After the EOT, esophageal varices and ALBI grade ≥2, remained associated with de novo PVT (subHR: 9.32; CI 95% 3.16-27.53 and subHR: 5.50; CI 95% 1.67-18.13, respectively).
CONCLUSIONS: In patients with HCV-related cirrhosis, a more advanced liver disease and significant portal hypertension are independently associated with the de novo PVT risk after SVR.